The principal objective of this proposal is to determine the mechanisms through which hormones interact to regulate a basic cell property: motility. This is represented by contractility of the uterine smooth muscle cells, in which we have previously characterized the alpha- and beta-adrenergic catecholamine receptors and described sex steroid hormone modulation of their membrane density and number. In the current year we will investigate the extent to which these changes explain altered uterine responsiveness to catecholamine stimulation during altered steroid hormone states. The effects of changes in receptor density on activation of beta-adrenergic catecholamine-sensitive adenylate cyclase will also be investigated especially with regard to possible functional interaction of the catecholamine receptor with other active agents such as prostaglandins and peptide hormones. The functional importance of modulating beta-adrenergic catecholamine-sensitive adenylate cyclase will be pursued further by investigating the consequences of hormone-induced redistribution of myometrial cAMP-dependent protein kinase. Translocation of this enzyme from the cytosol to a smooth muscle cell membrane fraction with sarcolemmal properties may be important in beta-adrenergic catecholamine receptor mediated events.